Rizatriptan 10mg tablets
Requires a prescription from a doctor or prescriber
Genetic variations that may affect drug response
1 known genetic variation may influence how your body responds to Rizatriptan 10mg tablets.Gene involved: GNB3
These are known genetic variations. They don't mean the medicine won't work for you — speak to your doctor or a pharmacogenomics specialist for personalised advice. Source: DrugBank (CC BY-NC 4.0).
Official documents, adverse reaction reporting, and safety monitoring
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Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
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Suspected adverse reactions reported for Rizatriptan
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
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Suspected adverse reactions reported for Rizatriptan
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
20 branded products available
Part of the Maxalt brand family (generic: Rizatriptan)
MHRA licensed products
View all licensed products for Rizatriptan on the MHRA register
Maxalt 10mg tablets
Maxalt 10mg tablets
Maxalt 10mg tablets
Rizatriptan 10mg tablets
Rizatriptan 10mg tablets
Rizatriptan 10mg tablets
Rizatriptan 10mg tablets
Rizatriptan 10mg tablets
Rizatriptan 10mg tablets
Rizatriptan 10mg tablets
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
WHO defined daily dose (DDD)
10 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
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Supply & safety information
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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 12 · Randomised trials: 1 · 2015–2026
Showing the 50 most relevant studies, sorted by most relevant.
Karlsson WK, Ostinelli EG, Zhuang ZA, et al.
2024
- Migraine Disorders
- Tryptamines
ObjectiveTo compare all licensed drug interventions as oral monotherapy for the acute treatment of migraine episodes in adults.DesignSystematic review and network meta-analysis.Data sourcesCochrane Central Register of Controlled Trials, Medline, Embase, ClinicalTrials.gov, EU Clinical Trials Register, WHO International Clinical Trials Registry Platform, as well as websites of regulatory agencies and pharmaceutical companies without language restrictions until 24 June 2023.MethodsScreening, data extraction, coding, and risk of bias assessment were performed independently and in duplicate. Random effects network meta-analyses were conducted for the primary analyses. The primary outcomes were the proportion of participants who were pain-free at two hours post-dose and the proportion of participants with sustained pain freedom from two to 24 hours post-dose, both without the use of rescue drugs. Certainty of the evidence was graded using the confidence in network meta-analysis (CINeMA) online tool. Vitruvian plots were used to summarise findings. An international panel of clinicians and people with lived experience of migraine co-designed the study and interpreted the findings.Eligibility criteria for selecting studiesDouble blind randomised trials of adults (≥18 years) with a diagnosis of migraine according to the International Classification of Headache Disorders.Results137 randomised controlled trials comprising 89 445 participants allocated to one of 17 active interventions or placebo were included. All active interventions showed superior efficacy compared with placebo for pain freedom at two hours (odds ratios from 1.73 (95% confidence interval (CI) 1.27 to 2.34) for naratriptan to 5.19 (4.25 to 6.33) for eletriptan), and most of them also for sustained pain freedom to 24 hours (odds ratios from 1.71 (1.07 to 2.74) for celecoxib to 7.58 (2.58 to 22.27) for ibuprofen). In head-to-head comparisons between active interventions, eletriptan was the most effective drug for pain freedom at two hours (odds ratios from 1.46 (1.18 to 1.81) to 3.01 (2.13 to 4.25)), followed by rizatriptan (1.59 (1.18 to 2.17) to 2.44 (1.75 to 3.45)), sumatriptan (1.35 (1.03 to 1.75) to 2.04 (1.49 to 2.86)), and zolmitriptan (1.47 (1.04 to 2.08) to 1.96 (1.39 to 2.86)). For sustained pain freedom, the most efficacious interventions were eletriptan and ibuprofen (odds ratios from 1.41 (1.02 to 1.93) to 4.82 (1.31 to 17.67)). Confidence in accordance with CINeMA ranged from high to very low. Sensitivity analyses on Food and Drug Administration licensed doses only, high versus low doses, risk of bias, and moderate to severe headache at baseline confirmed the main findings for both primary and secondary outcomes.ConclusionsOverall, eletriptan, rizatriptan, sumatriptan, and zolmitriptan had the best profiles and they were more efficacious than the recently marketed drugs lasmiditan, rimegepant, and ubrogepant. Although cost effectiveness analyses are warranted and careful consideration should be given to patients with a high risk cardiovascular profile, the most effective triptans should be considered as preferred acute treatment for migraine and included in the WHO List of Essential Medicines to promote global accessibility and uniform standards of care.Systematic review registrationOpen Science Framework https://osf.io/kq3ys/.
Abstract licence: CC BY
Cheng Y, Li J, Liu L, et al.
2026
BackgroundMigraine in children and adolescents not only impacts academic pursuits and family life but also have secondary psychological effects. Determining the role of acute medication for migraine treatment in this population can reduce the burden associated with migraine. This network meta-analysis aimed to identify the relative efficacy and safety of acute migraine drug in children and adolescents migraine populations.MethodsThe Cochrane Register of Controlled Trials and MEDLINE via PubMed and Embase databases were searched from inception to August 2025, only published studies in English. Double-blind randomized clinical trials evaluating the currently available acute treatments for childhood and adolescent migraines were included. The primary efficacy endpoint was pain freedom at 2 hours. Secondary efficacy endpoints included the proportion of participants with pain relief at 2 hours, pain freedom from two to 24 h, and the proportion using rescue drugs after 2 hours and up to 24 h. Adverse events (AEs) were also evaluated.ResultsThe analysis included 30 studies (involving 8,914 participants and 13 pharmacological interventions). All treatments included demonstrated higher odds ratios (ORs) compared with the placebo for pain freedom at 2 hours. Dihydroergotamine was associated with the highest ORs, but its confidence interval included null values. Sumatriptan/naproxen sodium, ibuprofen, zolmitriptan nasal spray, sumatriptan nasal spray, and rizatriptan showed statistical significance. Sumatriptan/naproxen sodium yielded the highest odds (OR: 2.91, 95% CI: 1.87-4.53), followed by ibuprofen (OR: 2.88, 95% CI: 1.47-5.64), and rizatriptan showed the lowest (OR: 1.51, 95% CI: 1.23-1.86). Only sumatriptan/naproxen sodium was associated with a significantly higher OR compared with placebo for pain freedom from two to 24 h (OR: 2.31, 95% CI: 1.31-4.07). Ibuprofen exhibited the highest effect size for pain relief at 2 hours (OR: 3.21, 95% CI: 1.10-9.34). None of the included drugs was found to reduce the use of rescue drugs from two to 24 h. Zolmitriptan was associated with the highest risk of AEs among all treatments. Acetaminophen appears to have the lowest risk of adverse events, comparable to that of a placebo.ConclusionIbuprofen can effectively relieve symptoms, characterized by a favorable benefit-risk profile. Sumatriptan and zolmitriptan nasal sprays also exhibited robust efficacy, specifically among populations with prominent nausea and vomiting. Sumatriptan/naproxen sodium merits consideration, especially in patients exhibiting an inadequate response to monotherapy. Dihydroergotamine demonstrated potential benefits in refractory and chronic migraine; however, high-quality studies are warranted to validate these findings.
Abstract licence: CC BY
Song Z, Guo Y, Gu J, et al.
2025
IntroductionMenstrual migraine (MM) is a common subtype of migraine that greatly affects a woman's quality of life. A number of different drugs are used to treat menstrual migraine, but it is not known which is more effective.MethodsIn this study, we searched all randomized controlled trials that satisfied the inclusion and exclusion criteria up to December 2023 on PubMed, Embase and Cochrane Library using a suitable search strategy. We constructed a suitable network model for analysis after evaluating the heterogeneity among the included direct, indirect and pooled evidence. Odds ratio (OR) and corresponding 95% confidence intervals (CI) were used as valid indicators for this network meta-analysis.ResultsIn the Bayesian network model we constructed, we found that lasmiditan (vs. placebo OR, 14; 95% CI 3.1-100) was better than rizatriptan (vs. placebo OR, 1.9; 95% CI 1.2-3.3) in terms of the rate of sustained freedom from pain. There was no statistically significant difference between lasmiditan and different triptans in terms of the rate of being pain-free at 2 h (2-h pain-free) and the rate of pain relief at 2 h (2-h pain relief). Regarding safety, the probability of adverse events was significantly higher for rizatriptan (OR, 2.7; 95% CI 1.1-7.3) than for placebo.ConclusionIn terms of treatment efficacy for MM, lasmiditan was not worse than different triptans and was even better than some of the triptans in the rate of sustained freedom from pain. As an emerging treatment, lasmiditan is promising for the treatment of MM. However, more research needs to be carried out because of the lack of safety analysis for lasmiditan.
Abstract licence: CC BY-NC
Jeffrey P. Staab, Scott D. Eggers, Joanna C. Jen, et al.
JAMA neurology, 2025
- Vestibular Diseases
- Tryptamines
- Triazoles
Vandana Bhatia, Vir Vikram, Aditya Rattan, et al.
Inflammopharmacology, 2025
- Tryptamines
- Triazoles
- Calcitonin Gene-Related Peptide
C. Göbel, A. Heinze, A. Cirkel, et al.
Pain and Therapy, 2024
Tepper SJ, Jenkins A, Henriksen C, et al.
2025
- Tryptamines
- Piperidines
- Pyridines
BackgroundThis study compared persistence of patients initiating rimegepant versus oral triptans for the acute treatment of migraine.MethodsA retrospective cohort analysis was conducted using US MarketScan claims data (1 March 2019 to 30 June 2023) among commercially- and US federal Medicare-insured migraine patients initiating rimegepant or oral triptans. Persistence was defined as having ≥1 refill within 12 months of initial prescription and was compared between propensity score-matched rimegepant and triptan cohorts.ResultsBefore matching, 13,599 patients were identified in the rimegepant cohort and 38,127 in the triptan cohort. After matching, each cohort included 9909 patients. Significantly more rimegepant patients were persistent (75.8%) versus triptan patients (53.5%) (odds ratio [OR] 2.72, 95% confidence interval [CI] 2.56-2.90). Subgroup analyses showed similar trends for rimegepant versus specific triptans (rizatriptan: OR 2.49 [95% CI 2.33-2.67], and sumatriptan: OR 2.92 [95% CI 2.73-3.12]) and in patients with chronic migraine (OR 2.86 [95% CI 2.53-3.23]).ConclusionsThis study provides compelling evidence that rimegepant is associated with greater persistence than oral triptans for real-world acute treatment of migraine. Rimegepant is a favorable option for patients seeking effective and tolerable long-term treatment, particularly for those with insufficient response, intolerability, or contraindications to triptans.
Abstract licence: CC BY-NC
Okazaki Y, Hori S, Takagi R, et al.
2025
Reversible cerebral vasoconstriction syndrome is characterized by severe headaches and diffuse, segmental constriction of cerebral arteries. We report a rare pediatric case of triptan-induced reversible cerebral vasoconstriction syndrome, complicated by both subarachnoid hemorrhage and cerebral infarction. A 10-year-old boy presented with persistent severe headaches initially suspected to be migraines, for which he was prescribed rizatriptan. Five days after starting rizatriptan, he developed impaired consciousness (Japan Coma Scale 10) and partial right-sided hemiparesis, prompting emergency hospitalization. A head computed tomography scan revealed subarachnoid hemorrhage in the left frontal cortical region. Cerebral angiography showed stenotic changes in the internal carotid artery, middle cerebral artery, anterior cerebral artery, and posterior cerebral artery. Suspecting triptan-induced reversible cerebral vasoconstriction syndrome, rizatriptan was discontinued, and verapamil treatment was initiated. Subsequent magnetic resonance imaging and magnetic resonance angiography revealed cerebral infarction in the right cerebellum, left middle cerebral artery territory, and right occipital lobe, with persistent stenotic changes from earlier findings. Edaravone was added to the treatment regimen. The patient's condition gradually improved, and follow-up magnetic resonance angiography showed almost complete resolution of the prior stenotic changes. His partial right-sided hemiparesis nearly resolved, and he was discharged home. Triptans should be used with caution, as they may precipitate reversible cerebral vasoconstriction syndrome or exacerbate cerebral vasoconstriction. Careful monitoring and vascular imaging are essential for patients presenting with symptoms following triptan administration.
Abstract licence: CC BY-NC-ND
Al-Saadi R, Mohammed Jawad ZJ, Khalaf OH, et al.
2025
- Nitroglycerin
- Tryptamines
- Triazoles
I. Dunaieva, P. Kravchun, O. Kryvoshapka, et al.
Bulletin of Problems Biology and Medicine, 2026
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
136 found
Half-life
Not available
Mechanism
There are several physiological and molecular processes implicated in the pathophysiology of migraine.
Food interactions
1 warning
Human targets
6 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
90%
Half-life
[L46018]
Protein binding
14%
[L46018]
Volume of distribution
140 L
[L46018]
Metabolism
14%
Elimination
10 mg
Clearance
1042 mL/min
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L46018][L46023][L46038][L46043]
Rizatriptan is not indicated for the prophylactic therapy of migraine nor the treatment of cluster headache.
[L46018]
In Canada, rizatriptan is approved in adults.
[L46038][L46043]
In the US, the oral tablet formulations are used in patients six years of age and older [L46018] and the oral film formation is approved for patients 12 years of age and older weighing 40 kg or more.
[L46023]
Rizatriptan, in combination with [Meloxicam] is indicated for the acute treatment of migraine with or without aura in adults.
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1226 interactions
[L46028]
No overdoses of rizatriptan were reported in clinical trials. Some adult patients who received 40 mg of rizatriptan either a single dose or as two doses with a two-hour interdose interval had dizziness and somnolence. Syncope, dizziness, bradycardia including third degree AV block, vomiting, and/or incontinence were experienced by two adults who received a total cumulative doses of 80 mg (given within four hours) in a clinical pharmacology study.
Some adolescent patients (aged 12 to 17 years old) receiving two 10-mg doses of orally disintegrating tablets of rizatriptan experienced abdominal discomfort, fatigue, and dyspnea.
[L46018]
Based on the pharmacological properties of rizatriptan, hypertension and myocardial ischemia are possible after overdosage. Gastrointestinal decontamination, (i.e., gastric lavage followed by activated charcoal) should be considered in patients suspected of an overdose with rizatriptan. Clinical and electrocardiographic monitoring should be continued for at least 12 hours, even if clinical symptoms are not observed.
The effects of hemo- or peritoneal dialysis on serum concentrations of rizatriptan are unknown.
[L46018]
Rizatriptan is a selective agonist at the 5-HT1B and 5-HT1D receptors on intracranial blood vessels and sensory nerves of the trigeminal system. It binds to these receptors with high affinity.[L46018] The exact mechanism of action of rizatriptan has not been fully elucidated; however, several documented pharmacological actions of rizatriptan may contribute to its antimigraine effects. Rizatriptan causes vasoconstriction of intracranial extracerebral blood vessels, which is thought to occur primarily via 5-HT1B receptors. Rizatriptan also inhibits nociceptive neurotransmission in trigeminal pain pathways. It attenuates the release of vasoactive neuropeptides by the trigeminal nerve, which is thought to occur via neurogenic and central 5-HT1D receptors.[A1460][A258918][A258928] Rizatriptan inhibited neurogenic dural vasodilation and plasma protein extravasation in animal studies.[A1460][A5971][A258918][A258928]
Rizatriptan has a weak affinity for other 5-HT1 receptor subtypes (5-HT1A, 5-HT1E, 5-HT1F) and the 5-HT7 receptor but has no significant activity at 5-HT2, 5-HT3, alpha- and beta-adrenergic, dopaminergic, histaminergic, muscarinic or benzodiazepine receptors.[L46038]
How the body processes this drug — absorption, distribution, metabolism, and elimination
Food has no significant effect on the bioavailability of rizatriptan but delays the time to reach peak concentration by an hour. In clinical trials, rizatriptan was administered without regard to food.
[L46018]
The bioavailability and Cmax of rizatriptan were similar following the administration of rizatriptan tablets and rizatriptan orally disintegrating tablets. Still, the absorption rate is somewhat slower with orally disintegrating tablets, with Tmax delayed by up to 0.7 hours.
The AUC of rizatriptan is approximately 30% higher in females than males. No accumulation occurred on multiple dosing.
[L46018]
[L46018]
[L46018]
[L46018]
Other pharmacologically inactive minor metabolites include the N-oxide, the 6-hydroxy compound, and the sulfate conjugate of the 6-hydroxy metabolite.
[A1460][A258963][L46018]
[L46018]
[A258918][A258923]
Proteins and enzymes this drug interacts with in the body
PMID:10452531 PMID:1315531 PMID:1328844 PMID:1348246 PMID:1351684 PMID:1559993 PMID:1565658 PMID:1610347 PMID:23519210 PMID:23519215 PMID:29925951 PMID:8218242
Also functions as a receptor for ergot alkaloid derivatives, various anxiolytic and antidepressant drugs and other psychoactive substances, such as lysergic acid diethylamide (LSD) .
PMID:23519210 PMID:23519215 PMID:29925951
Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors, such as adenylate cyclase .
PMID:10452531 PMID:1315531 PMID:1328844 PMID:1348246 PMID:1351684 PMID:1559993 PMID:1565658 PMID:1610347 PMID:23519210 PMID:23519215 PMID:29925951 PMID:8218242
HTR1B is coupled to G(i)/G(o) G alpha proteins and mediates inhibitory neurotransmission by inhibiting adenylate cyclase activity .
PMID:29925951 PMID:35610220
Arrestin family members inhibit signaling via G proteins and mediate activation of alternative signaling pathways .
PMID:29925951
Regulates the release of 5-hydroxytryptamine, dopamine and acetylcholine in the brain, and thereby affects neural activity, nociceptive processing, pain perception, mood and behavior .
PMID:18476671 PMID:20945968
Besides, plays a role in vasoconstriction of cerebral arteries PMID:15853772
PMID:10452531 PMID:1565658 PMID:1652050 PMID:33762731
Also functions as a receptor for ergot alkaloid derivatives, various anxiolytic and antidepressant drugs and other psychoactive substances .
PMID:10452531 PMID:1565658 PMID:1652050 PMID:33762731
Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors, such as adenylate cyclase .
PMID:10452531 PMID:1565658 PMID:1652050 PMID:33762731
HTR1D is coupled to G(i)/G(o) G alpha proteins and mediates inhibitory neurotransmission by inhibiting adenylate cyclase activity .
PMID:33762731
Regulates the release of 5-hydroxytryptamine in the brain, and thereby affects neural activity .
PMID:18476671 PMID:20945968
May also play a role in regulating the release of other neurotransmitters .
PMID:18476671 PMID:20945968
May play a role in vasoconstriction PMID:18476671 PMID:20945968
PMID:21422162 PMID:34239069 PMID:8380639 PMID:8384716
Also functions as a receptor for various alkaloids and psychoactive substances .
PMID:21422162 PMID:8380639 PMID:8384716
Receptor for lasmiditan, a drug for the treatment of acute migraine .
PMID:34239069
Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors, such as adenylate cyclase .
PMID:34239069
HTR1F is coupled to G(i)/G(o) G alpha proteins and mediates inhibitory neurotransmission by inhibiting adenylate cyclase activity PMID:34239069 PMID:35610220
PMID:35714614 PMID:8226867
Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors .
PMID:35714614 PMID:8226867
HTR7 is coupled to G(s) G alpha proteins and mediates activation of adenylate cyclase activity PMID:35714614
PMID:22957663 PMID:3138543 PMID:33762731 PMID:37935376 PMID:37935377 PMID:8138923 PMID:8393041
Also functions as a receptor for various drugs and psychoactive substances .
PMID:22957663 PMID:3138543 PMID:33762731 PMID:38552625 PMID:8138923 PMID:8393041
Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors, such as adenylate cyclase .
PMID:22957663 PMID:3138543 PMID:33762731 PMID:8138923 PMID:8393041
HTR1A is coupled to G(i)/G(o) G alpha proteins and mediates inhibitory neurotransmission: signaling inhibits adenylate cyclase activity and activates a phosphatidylinositol-calcium second messenger system that regulates the release of Ca(2+) ions from intracellular stores .
PMID:33762731 PMID:35610220
Beta-arrestin family members regulate signaling by mediating both receptor desensitization and resensitization processes .
PMID:18476671 PMID:20363322 PMID:20945968
Plays a role in the regulation of 5-hydroxytryptamine release and in the regulation of dopamine and 5-hydroxytryptamine metabolism .
PMID:18476671 PMID:20363322 PMID:20945968
Plays a role in the regulation of dopamine and 5-hydroxytryptamine levels in the brain, and thereby affects neural activity, mood and behavior .
PMID:18476671 PMID:20363322 PMID:20945968
Plays a role in the response to anxiogenic stimuli PMID:18476671 PMID:20363322 PMID:20945968
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC N02CC04
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Rizatriptan
Additional database identifiers
Drugs Product Database (DPD)
11899
ChemSpider
4900
BindingDB
50033437
Guide to Pharmacology
51
ZINC
ZINC000000005895
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5287
GenAtlas
HTR1B
GeneCards
HTR1B
GenBank Gene Database
D10995
GenBank Protein Database
219679
Guide to Pharmacology
2
UniProt Accession
5HT1B_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5289
GenAtlas
HTR1D
GeneCards
HTR1D
GenBank Gene Database
M89955
GenBank Protein Database
177772
Guide to Pharmacology
3
UniProt Accession
5HT1D_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5292
GenAtlas
HTR1F
GeneCards
HTR1F
GenBank Gene Database
L05597
GenBank Protein Database
307420
Guide to Pharmacology
5
UniProt Accession
5HT1F_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5302
GenAtlas
HTR7
GeneCards
HTR7
GenBank Gene Database
U68487
GenBank Protein Database
1857143
Guide to Pharmacology
12
UniProt Accession
5HT7R_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5286
GenAtlas
HTR1A
GeneCards
HTR1A
GenBank Gene Database
M28269
GenBank Protein Database
189928
Guide to Pharmacology
1
UniProt Accession
5HT1A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5291
GenAtlas
HTR1E
GeneCards
HTR1E
GenBank Gene Database
M91467
GenBank Protein Database
177774
Guide to Pharmacology
4
UniProt Accession
5HT1E_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6833
GenAtlas
MAOA
GeneCards
MAOA
GenBank Gene Database
M68840
GenBank Protein Database
187353
Guide to Pharmacology
2489
UniProt Accession
AOFA_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2625
GenAtlas
CYP2D6
GeneCards
CYP2D6
GenBank Gene Database
M20403
GenBank Protein Database
181350
Guide to Pharmacology
1329
UniProt Accession
CP2D6_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72